Evidence map›Paper›PMID 24632433›Full record

ArticleNeurotoxicology and teratology

The Notch target E(spl)mδ is a muscle-specific gene involved in methylmercury toxicity in motor neuron development.

Gregory L Engel, Matthew D Rand

Erratum issuedOpen access · greenAbstract read
In one paragraph

Article in Neurotoxicology and teratology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.6field-weighted citation impact, top 33% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

14 citing papers in PubMed, 20 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Neuroligin-1 Is a Mediator of Methylmercury Neuromuscular Toxicity.Toxicological sciences : an official journal of the Society of Toxicology · 2021
    Article
  5. Article
  6. Article
  7. Review
  8. Methylmercury modifies temporally expressed myogenic regulatory factors to inhibit myoblast differentiation.Toxicology in vitro : an international journal published in association with BIBRA · 2020
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

2 authors at 2 institutions in 1 country.

Gregory L EngelDepartment of Anatomy and Neurobiology, College of Medicine, University of Vermont, Burlington, VT 05405, United States.
Matthew D RandDepartment of Environmental Medicine, University of Rochester School of Medicine and Dentistry, 601 Elmwood Ave., Box EHSC, Rochester, NY 14622, United States.
University of Rochester · USUniversity of Vermont · US

Funding

VISUAL INDICES OF NEUROTOXICITYP30ES001247 · NIEHS · UNIVERSITY OF ROCHESTER · PI Martha Susiarjo · 1985 to 2026
$42.8M
ENVIRONMENTAL PATHOLOGY TRAINING PROGRAMT32ES007122 · NIEHS · UNIVERSITY OF VERMONT &ST AGRIC COLLEGE · PI VAN DER VLIET, ALBERT · 1985 to 2012
$4.2M
Mechanisms of methylmercury toxicity in neural developmentR01ES015550 · NIEHS · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI RAND, MATTHEW D · 2007 to 2011
$1.4M
Neurotoxicity of methylmercury in Drosophila embryo developmentR03ES021581 · NIEHS · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI RAND, MATTHEW D · 2012 to 2013
$151k
NIEHS NIH HHS P30 ES001247NIEHS NIH HHS R01 ES015550NIEHS NIH HHS R01-ES015550NIEHS NIH HHS R03 ES021581NIEHS NIH HHS R03-ES021581NIEHS NIH HHS T32 ES007122NIEHS NIH HHS T32-ES07122
6 · The paper itself

Abstract

Methylmercury (MeHg) is a ubiquitous environmental toxin that has a selective and potent impact on the nervous system, particularly during neural development yet, the mechanisms for its apparent neurodevelopmental specificity are unknown. The Notch receptor pathway has been implicated as a MeHg target in several studies. Notch signaling mediates cell-cell signals in a number of developmental contexts including neurogenesis and myogenesis, where it fundamentally acts to repress differentiation. Previous work in our lab has shown that MeHg causes preferential upregulation of a canonical Notch response gene, E(spl)mδ, in Drosophila embryos. In parallel, MeHg is seen to disrupt outgrowth of embryonic intersegmental motor nerves (ISN), which can be mimicked by expression of activated Notch in embryonic neurons. However, overexpression of E(spl)mδ in developing neurons fails to elicit motor neuron outgrowth defects, pointing to a non-autonomous role for E(spl)mδ in motor axon development. In this study we investigate a role for E(spl)mδ in conveying the toxicity of MeHg in the embryo. We find that endogenous expression of the E(spl)mδ gene localizes to developing somatic muscles in embryos. Notably, E(spl)mδ expression is seen in several muscles that are known synaptic targets for both the ISN and the segmental motor nerve (SN). We also demonstrate that the SN, similar to the ISN, exhibits disrupted axon outgrowth in response to MeHg. E(spl)mδ can induce a SN motor neuron phenotype, similar to MeHg treatment; but, only when E(spl)mδ expression is targeted to developing muscles. E(spl)mδ overexpression in developing muscles also results in aberrant muscle morphology, which is not apparent with expression of the closely related E(spl)mγ in developing muscles. Our data point to a role for the Notch target E(spl)mδ in mediating MeHg toxicity in embryonic development by disrupting the coordinated targeting of motor neurons to their muscle targets.

Indexed as

MusclesAnimalsAnimals, Genetically ModifiedBasic Helix-Loop-Helix ProteinsDrosophilaDrosophila ProteinsEmbryonic DevelopmentEmbryo, NonmammalianGene Expression Regulation, DevelopmentalGreen Fluorescent ProteinsMethylmercury CompoundsMotor NeuronsPeripheral NervesReceptors, NotchRepressor ProteinsBasic Helix-Loop-Helix ProteinsDrosophila ProteinsE(spl)mdelta-HLH protein, DrosophilaGreen Fluorescent ProteinsMethylmercury CompoundsReceptors, NotchRepressor ProteinsDrosophila embryoEnhancer of splitMethylmercuryMotor neuronMyogenesisNotch

Identifiers

PMID24632433
PMCPMC4043954
OpenAlexW2031225247

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.